000142466 001__ 142466
000142466 005__ 20240229105148.0
000142466 0247_ $$2doi$$a10.1080/10428194.2018.1443450
000142466 0247_ $$2pmid$$apmid:29616856
000142466 0247_ $$2ISSN$$a1026-8022
000142466 0247_ $$2ISSN$$a1029-2403
000142466 0247_ $$2ISSN$$a1042-8194
000142466 0247_ $$2altmetric$$aaltmetric:35725888
000142466 037__ $$aDKFZ-2019-00185
000142466 041__ $$aeng
000142466 082__ $$a610
000142466 1001_ $$0P:(DE-He78)8dc0876dc3ed1862337d98842984727d$$aLehners, Nicola$$b0$$eFirst author$$udkfz
000142466 245__ $$aOncogene-induced senescence: a potential breakpoint mechanism against malignant transformation in plasma cell disorders.
000142466 260__ $$aLondon [u.a.]$$bTaylor & Francis Group$$c2018
000142466 3367_ $$2DRIVER$$aarticle
000142466 3367_ $$2DataCite$$aOutput Types/Journal article
000142466 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1550145333_26424
000142466 3367_ $$2BibTeX$$aARTICLE
000142466 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000142466 3367_ $$00$$2EndNote$$aJournal Article
000142466 520__ $$aOncogene-induced senescence (OIS) is a cellular tumor-suppressive mechanism present in several premalignant conditions. Here, we analyze the possible impact of OIS on malignant transformation in plasma cell disorders. Tumor samples from 125 patients with different disease stages were analyzed immunohistochemically for expression of senescence markers. Protein expression of cyclin-dependent kinase inhibitor p21Cip1/Waf1 was significantly higher in smoldering multiple myeloma (SMM) compared to monoclonal gammopathy of undetermined significance (MGUS) (p = .02) or symptomatic multiple myeloma (MM) (p = .005). SMM plasma cells expressing p21Cip1/Waf1 were negative for Ki67, consistent with senescence. While p27Kip1 was highly expressed in healthy controls, MGUS and SMM, expression decreased significantly in MM (p = .02). SMM plasma cells displayed a mutually exclusive expression of p21Cip1/Waf1/p27Kip1 suggesting compensatory mechanisms of senescence. In conclusion, we found markers of cellular senescence differentially expressed in SMM compared to MGUS and MM supporting the hypothesis of OIS as a breakpoint mechanism against malignant transformation in plasma cell disorders.
000142466 536__ $$0G:(DE-HGF)POF3-317$$a317 - Translational cancer research (POF3-317)$$cPOF3-317$$fPOF III$$x0
000142466 588__ $$aDataset connected to CrossRef, PubMed,
000142466 7001_ $$aEllert, Elena$$b1
000142466 7001_ $$0P:(DE-He78)f679da0a40ea99b8fe8252161559a68b$$aXu, Jing$$b2$$udkfz
000142466 7001_ $$aHillengass, Jens$$b3
000142466 7001_ $$aLeichsenring, Jonas$$b4
000142466 7001_ $$aStenzinger, Albrecht$$b5
000142466 7001_ $$aGoldschmidt, Hartmut$$b6
000142466 7001_ $$aAndrulis, Mindaugas$$b7
000142466 7001_ $$0P:(DE-He78)1cb537e833afd985097ccfaddffb2ef3$$aRaab, Marc-Steffen$$b8$$eLast author$$udkfz
000142466 773__ $$0PERI:(DE-600)2030637-4$$a10.1080/10428194.2018.1443450$$gVol. 59, no. 11, p. 2660 - 2669$$n11$$p2660 - 2669$$tLeukemia and lymphoma$$v59$$x1029-2403$$y2018
000142466 909CO $$ooai:inrepo02.dkfz.de:142466$$pVDB
000142466 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)8dc0876dc3ed1862337d98842984727d$$aDeutsches Krebsforschungszentrum$$b0$$kDKFZ
000142466 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)f679da0a40ea99b8fe8252161559a68b$$aDeutsches Krebsforschungszentrum$$b2$$kDKFZ
000142466 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)1cb537e833afd985097ccfaddffb2ef3$$aDeutsches Krebsforschungszentrum$$b8$$kDKFZ
000142466 9131_ $$0G:(DE-HGF)POF3-317$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vTranslational cancer research$$x0
000142466 9141_ $$y2018
000142466 915__ $$0StatID:(DE-HGF)0420$$2StatID$$aNationallizenz
000142466 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000142466 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000142466 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000142466 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bLEUKEMIA LYMPHOMA : 2017
000142466 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search
000142466 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC
000142466 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List
000142466 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000142466 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000142466 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine
000142466 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences
000142466 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5
000142466 9201_ $$0I:(DE-He78)G170-20160331$$kG170$$lExperimentelle Therapien hämatologischer Neoplasien$$x0
000142466 980__ $$ajournal
000142466 980__ $$aVDB
000142466 980__ $$aI:(DE-He78)G170-20160331
000142466 980__ $$aUNRESTRICTED